DNA and Oxidative Damages Decrease After Ingestion of Folic Acid in Patients with Type 2 Diabetes
Background and Aims Type 2 diabetes mellitus (T2DM) is a chronic degenerative disease that promotes autoxidation of sugars, leading to the production of reactive oxygen species. This damage occurs especially at the level of cellular proteins, carbohydrates, lipids and DNA, thus playing an important...
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Published in | Archives of medical research Vol. 43; no. 6; pp. 476 - 481 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
01.08.2012
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Subjects | |
Online Access | Get full text |
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Summary: | Background and Aims Type 2 diabetes mellitus (T2DM) is a chronic degenerative disease that promotes autoxidation of sugars, leading to the production of reactive oxygen species. This damage occurs especially at the level of cellular proteins, carbohydrates, lipids and DNA, thus playing an important role in the pathogenesis of late complications of T2DM. We investigated the effect of folic acid on DNA and oxidative damage in patients with T2DM. Methods We studied 30 individuals diagnosed with T2DM and 30 control individuals without disease. Individuals with T2DM were prescribed 5 mg of folic acid, taken orally three times daily for 1 month. Samples were taken 15 and 30 days after treatment. DNA damage was determined using the micronucleus test in oral mucosa and oxidative stress by quantifying 8-hydroxy-2′-deoxyguanosine (8-OHdG) as well as by quantifying total lipid peroxides. Results Individuals with T2DM had a higher number of micronuclei as well as higher levels of 8-OHdG and lipid peroxides than the control group ( p = 0.001). Individuals with T2DM showed a significant reduction in the number of micronuclei and the concentration of 8-OHdG and lipid peroxides over time with folic acid intake. Conclusions A positive correlation exists between oxidative stress produced by T2DM and DNA damage, so the use of an antioxidant such as folic acid in DM2 therapy is advisable for delaying complications due to T2DM-induced oxidative stress and DNA damage. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Article-2 ObjectType-Feature-1 |
ISSN: | 0188-4409 1873-5487 |
DOI: | 10.1016/j.arcmed.2012.08.013 |